https://scholars.lib.ntu.edu.tw/handle/123456789/147005
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor | 臺大醫學院-醫學檢驗暨生物技術學系暨研究所; | - |
dc.contributor.author | Su, Te-Jen | en |
dc.contributor.author | Ku, Wen-Hui | en |
dc.contributor.author | Chen, Hsuan-Yu | en |
dc.contributor.author | Hsu, Yi-Chiung | en |
dc.contributor.author | Hong, Qi-Sheng | en |
dc.contributor.author | Chang, Gee-Chen | en |
dc.contributor.author | Yu, Sung-Liang | en |
dc.contributor.author | Chen, Jeremy J. W. | en |
dc.creator | Su, Te-Jen;Ku, Wen-Hui;Chen, Hsuan-Yu;Hsu, Yi-Chiung;Hong, Qi-Sheng;Chang, Gee-Chen;Yu, Sung-Liang;Chen, Jeremy J. W. | en |
dc.creator | 俞松良 | zh-tw |
dc.date | 2016 | - |
dc.date.accessioned | 2017-06-30T04:39:11Z | - |
dc.date.accessioned | 2018-07-06T08:42:28Z | - |
dc.date.available | 2017-06-30T04:39:11Z | - |
dc.date.available | 2018-07-06T08:42:28Z | - |
dc.date.issued | 2016 | - |
dc.identifier.uri | http://ntur.lib.ntu.edu.tw//handle/246246/280943 | - |
dc.description.abstract | Although targeted therapy can prolong the survival of non-small cell lung cancer (NSCLC) patients with EGFR mutations, chemotherapy still is the choice for patients with wild-type EGFR or failure in targeted therapy. However, most of the patients will eventually develop chemoresistance. Our previous study showed that miR-137 is a risky microRNA and is associated with poor prognosis in NSCLC patients. Here we investigated the role of miR-137 in cisplatin resistance in lung adenocarcinoma patients. Our data indicated that miR-137 overexpression increases the survival of lung cancer cells exposed to cisplatin and decreases cisplatin-induced apoptosis. Through computational prediction and microarray, we identified caspase-3 (CASP3) as a potential target of miR-137. Luciferase reporter and site-directed mutagenesis assays demonstrated that miR-137 downregulates CASP3 through binding to its 3'-UTR. Moreover, the endogenous CASP3 can be modulated by overexpressing or silencing miR-137 in lung adenocarcinoma cell lines regardless of EGFR status. Suppression of CASP3 by miR-137 provides cancer cells with anti-apoptotic ability, leading to cisplatin resistance. Immunohistochemistry results revealed an inverse correlation between miR-137 and CASP3 expressions in lung adenocarcinoma patients. Together, our data provide a new chemoresistance mechanism in lung adenocarcinoma and a possible target to control chemoresistance in lung adenocarcinoma patients. | - |
dc.language | en-us | - |
dc.relation | Am. J. Cancer Res., 6(6), 1317-1330 | - |
dc.relation.ispartof | Am. J. Cancer Res. | - |
dc.subject | miR-137 | - |
dc.subject | lung adenocarcinoma | - |
dc.subject | cisplatin | - |
dc.subject | caspase 3 | - |
dc.subject | chemoresistance | - |
dc.subject.classification | [SDGs]SDG3 | - |
dc.title | Oncogenic miR-137 contributes to cisplatin resistance via repressing CASP3 in lung adenocarcinoma | - |
dc.relation.pages | 1317-1330 | - |
dc.relation.journalvolume | 6 | - |
dc.relation.journalissue | 6 | - |
item.fulltext | no fulltext | - |
item.grantfulltext | none | - |
顯示於: | 醫學檢驗暨生物技術學系 |
在 IR 系統中的文件,除了特別指名其著作權條款之外,均受到著作權保護,並且保留所有的權利。